Kv1.3 channel blockade enhances the phagocytic function of RAW264.7 macrophages

Zhu, Hong; Li, Yan; Gu, Jun; Hao, Wei; Cao, Ji‐Min

doi:10.1007/s11427-015-4915-3

Cited by 10 publications

(8 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Anti-phagocytic functions were determined using RAW264.7 cells (Anchorage-dependent cell, FH0328, FuHeng Cell Center, Shanghai, China), performed as previously described. 17 Briefly, 2×10 5 /mL RAW264.7 cells and 2×10 6 CFU/mL bacteria were incubated at 37°C for 1.5 hours. Trypan blue staining cell viability assay kit was used to determine viability of RAW264.7 cells.…”

Section: Methodsmentioning

confidence: 99%

Epidemic Potential of Escherichia coli O16:H41-ST131: Compared with Pandemic O25b:H30-ST131 Lineage

Zhang

Huang

et al. 2021

IDR

View full text Add to dashboard Cite

Background: O16:H41 is an important subclone among Escherichia coli (E. coli) sequence type (ST) 131, which has risen dramatically in recent years. However, reasons for the rapid increase of E. coli O16:H41-ST131 remain unclear. The aim of this study was to compare the pathogenicity and survivability features of E. coli O16:H41-ST131 with global epidemic O25b:H30-ST131 lineage. Methods: Sixteen E. coli ST131 were divided into two groups: group O16:H41-ST131 (n=6) and group O25b:H30-ST131 (n=10). Adhesion and invasion activity of different isolates were measured using human T24 cells. Biofilm production was quantified by crystal violet staining. Fifty percent human serum was used to detect serum sensitivity. Resistance to hydrogen peroxide was detected by broth microdilution method, and anti-phagocytic function was determined by phagocytosis experiments.Results: E. coli O16:H41-ST131 and O25b:H30-ST131 lineage showed similar biofilm formation, adhesion and invasion abilities. In terms of survivability, resistance to serum and hydrogen peroxide of E. coli O16:H41-ST131 was similar as that of E. coli O25b:H30-ST131. But anti-phagocytic function of E. coli O16:H41-ST131 was significantly weaker than that of E. coli O25b:H30-ST131. Conclusion:The pathogenicity and survivability of E. coli O16:H41-ST131 were similar to those of E. coli O25b:H30-ST131, which may be important reasons for its increasing prevalence. Our study may contribute to a better understanding of the prevalence of E. coli O16:H41-ST131.

show abstract

Section: Methodsmentioning

confidence: 99%

Epidemic Potential of Escherichia coli O16:H41-ST131: Compared with Pandemic O25b:H30-ST131 Lineage

Zhang

Huang

et al. 2021

IDR

View full text Add to dashboard Cite

show abstract

“…Monocytes may be one of the targets of statins, and the effects of statins on monocytes may be the possible mechanism underlying early intervention for atherosclerosis. Kv1.3 and KCa3.1 are two potassium channels that are consistently demonstrated to be associated with atherosclerosis (Kohler et al, 2003;Toyama et al, 2008;Zhu et al, 2015;Wu et al, 2015;Kan et al, 2016). Margatoxin (MgTX) can specifically block the Kv1.3 potassium current, and Tram-34 is a KCa3.1-specific blocking agent.…”

Section: Introductionmentioning

confidence: 99%

Pleiotropic Effects of Simvastatin on the Regulation of Potassium Channels in Monocytes

Wang

Ran²,

Chen

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Purpose: The underlying mechanism of pleiotropic effects of statins on atherosclerosis is still unclear. Kv1.3 and KCa3.1 are two potassium channels that might be involved in monocyte migration and atherosclerosis formation. The aim of this study was to investigate the effect of simvastatin on the Kv1.3 and KCa3.1 in monocyte.Methods and Results: In human monocytic THP-1 cells, simvastatin significantly inhibited Kv1.3 mRNA and protein expression by real-time quantitative PCR analysis and western blotting. However, simvastatin had no effects on KCa3.1 mRNA and protein expression. By whole-cell patch clamp, simvastatin (10 mM) remarkably inhibited the current intensity of Kv1.3, but had no effect on KCa3.1. Simvastatin (10 mM) treatment significantly reduced the monocyte chemoattractant protein 1 (MCP-1)-induced monocyte migration. This inhibition was only partially reversed by mevalonate (1mM). In human peripheral blood mononuclear cells (PBMCs), both Kv1.3 and KCa3.1 mRNA expression were increased in patients with coronary artery diseases (CAD) (n = 20) compared to healthy controls (n = 22). However, simvastatin (40 mg per day) significantly inhibited the Kv1.3 but not KCa3.1 mRNA expression after 1 month and 3 months therapy in CAD patients. Conclusion:Our data suggested Kv1.3 in monocytes was a potential molecular target of the pleiotropic effects of statins. KCa3.1 might be another marker of CAD, but not associated with statins treatment.

show abstract

“…Kv1.3 is highly expressed in activated macrophages and plays important roles in apoptosis, migration, phagocytosis, and immunomodulation of macrophages ( 12 , 13 , 14 , 15 ). To investigate whether FS48 had effects on the function of Kv channels of macrophages, the Kv currents evoked by depolarizing pulses in Raw 264.7 cells were measured under the administration of FS48.…”

Section: Resultsmentioning

confidence: 99%

Anti-inflammatory effects of FS48, the first potassium channel inhibitor from the salivary glands of the flea Xenopsylla cheopis

Deng

Zeng

Tang

et al. 2021

Journal of Biological Chemistry

View full text Add to dashboard Cite

Edited by Mike ShipstonThe voltage-gated potassium (Kv) 1.3 channel plays a crucial role in the immune responsiveness of T-lymphocytes and macrophages, presenting a potential target for treatment of immune-and inflammation related-diseases. FS48, a protein from the rodent flea Xenopsylla cheopis, shares the three disulfide bond feature of scorpion toxins. However, its threedimensional structure and biological function are still unclear. In the present study, the structure of FS48 was evaluated by circular dichroism and homology modeling. We also described its in vitro ion channel activity using patch clamp recording and investigated its anti-inflammatory activity in LPS-induced Raw 264.7 macrophage cells and carrageenaninduced paw edema in mice. FS48 was found to adopt a common αββ structure and contain an atypical dyad motif. It dose-dependently exhibited the Kv1.3 channel in Raw 264.7 and HEK 293T cells, and its ability to block the channel pore was demonstrated by the kinetics of activation and competition binding with tetraethylammonium. FS48 also downregulated the secretion of proinflammatory molecules NO, IL-1β, TNF-α, and IL-6 by Raw 264.7 cells in a manner dependent on Kv1.3 channel blockage and the subsequent inactivation of the MAPK/NF-κB pathways. Finally, we observed that FS48 inhibited the paw edema formation, tissue myeloperoxidase activity, and inflammatory cell infiltrations in carrageenantreated mice. We therefore conclude that FS48 identified from the flea saliva is a novel potassium channel inhibitor displaying anti-inflammatory activity. This discovery will promote understanding of the bloodsucking mechanism of the flea and provide a new template molecule for the design of Kv1.3 channel blockers.Voltage-gated potassium (Kv) channels play an important role in Ca 2+ signaling, action potential repolarization, cellular proliferation, migration and secretion, and cell volume

show abstract

Kv1.3 channel blockade enhances the phagocytic function of RAW264.7 macrophages

Cited by 10 publications

References 34 publications

Epidemic Potential of Escherichia coli O16:H41-ST131: Compared with Pandemic O25b:H30-ST131 Lineage

Epidemic Potential of Escherichia coli O16:H41-ST131: Compared with Pandemic O25b:H30-ST131 Lineage

Pleiotropic Effects of Simvastatin on the Regulation of Potassium Channels in Monocytes

Anti-inflammatory effects of FS48, the first potassium channel inhibitor from the salivary glands of the flea Xenopsylla cheopis

Contact Info

Product

Resources

About